It’s a hot summer night in the suburbs, most of which you’ve spent on standby for a local baseball game. After clearing up you’re put on a chest pain call a few blocks from your quarters. The local volunteer fire department has a squad on scene which is advising you to, “continue on emergency.”
Upon your arrival you find the patient seated on the porch, on O2 via a non-rebreather, in moderate respiratory distress. The volunteer EMT relays that the patient, a 59 year old male, is having 10 of 10 chest pressure which started yesterday. He’s administered 324 mg of aspirin and withheld nitroglycerin because of the patient’s blood pressure. You’re handed a quick trip sheet as you take over patient care.
- Pulse: 50, weak at the radials
- BP: 80/40
- RR: 24, labored, lungs clear and equal bilaterally
- SpO2: 90% on room air, 94% on 15 L/min via NRB
Your partner starts putting on the electrodes for a 12-Lead while you get a quick history.
- PMHx: hypertension, hypercholesterolemia, GERD
- Medications: lisinopril, lipitor, omeprazole, “vitamins”
- Allergies: penicillin, sulfa drugs, levitra
- Last ins/outs: normal dinner
The patient appears acutely unwell, ashen gray, and diaphoretic. He states the pain is, “pretty constant now,” and that he feels it in, “my shoulder blades and running down my spine”. Your partner hands you the initial 12-Lead:
The EMT helps you and your partner place the patient on your stretcher and move the patient to your unit. Your partner asks you what you think about the 12-Lead and if you’ll need a driver.
- What does the 12-Lead show?
- Should this patient be taken to the local hospital, about 10 minutes away, or the cardiac center, about 25 minutes away?
- Do you need a driver?
When we left off, weâ€™d loaded our 59 year old male patient with 10 of 10 chest pressure into the back of our unit with the help of a local volunteer EMT. The patient appeared acutely unwell and was hypotensive and bradycardic.
Before we discuss the ECG in depth, letâ€™s show a serial 12-Lead the crew obtained shortly after leaving the scene.
The importance of serial ECGâ€™s cannot be overstated.Â Using only one prehospital ECG could miss nearly 20% of all STEMI patients!
At this point we can see an obvious inferoposterior STEMI, likely due to an RCA occlusion. Also of note is a new right bundle branch block, which is an ominous sign. These changes were not lost on the crew, and the receiving facility, a PCI center, was made aware.
However, during their radio report a rhythm change was noted on the monitor:
A single R-on-T PVC is seen initiating ventricular fibrillation. Thankfully, the crew elected to use a driver and had two sets of hands in the back. The defibrillator was charged while CPR was initiated, and a 200J shock was delivered after a period of chest compressions:
A rhythm change was noted, however, as no pulses were present chest compressions were continued:
Within a minute the patient awoke during CPR, and regained full consciousness. A repeat 12-Lead was obtained:
This ECG shows sinus tachycardia, right bundle branch block, and the evolving inferoposterior STEMI. Upon arrival at the PCI center, the patient was pit stopped in the EDâ€™s resuscitation bay due to his recent ventricular arrhythmia. While there, he experienced another VF arrest. He was again resuscitated and moved to the cath lab for PCI.
Could we have predicted this series of events from the initial ECG?Â Yes and no.
Yes, the initial ECG provided all of the findings necessary to determine that the patient was experiencing a coronary artery occlusion.Â Reciprocal changes or T-wave inversion in aVL is an earlier and more sensitive finding than inferior ST-elevation during acute inferior STEMI.
No, the VF arrest is not as predictable. The R-on-T PVC which initiated ventricular fibrillationÂ was theÂ onlyÂ PVCÂ found on the full cardiac monitor report prior to the arrest!Â However, it is a best practice to place multifunction electrode pads on any STEMI patient in anticipation for these events.
Looking back the initial ECG we can see why the arbitrary criteria of 1 mm ST-elevation is not nearly sensitive enough to catch every coronary artery occlusion:
- Hyperacute T-waves dominate the inferior leads
- T-wave inversion in aVL
- ST-depression in I, V2, V3, and V4
- Subtle ST-elevation relative to the PR-segment in III, aVF, and V6 (the actual isoelectric baseline)
Remember, ST-depression due to ischemiaÂ does not localize.Â Localized ST-depression is a reciprocal change until proven otherwise!
During PCI the patient was found to have a 99% occlusion of the LCX and received one stent.
Even with two VF arrests, theÂ time from first medical contact to balloon was 61 minutes! If you do not believe in a system of care which begins with dispatchers, first responders, and EMS, travels through the hospital, and ends up back with EMS through continuous quality improvement feedback, perhaps this case can change your mind.
- Verbeek PR, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehosp Emerg Care. 2012; 16(1):109-14. [PubMed]
- Smith SW. Inferior Hyperacute T-waves. Dr. Smithâ€™s ECG Blog, published 26 August 2009. [Free Full Text]
- Smith SW. Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation. Dr. Smithâ€™s ECG Blog, published 8 February 2011. [Free Full Text]
- Smith SW. A Male in his 60s with Chest pain. What is the ECG Diagnosis? Dr. Smithâ€™s ECG Blog, published 13 December 2013. [Free Full Text]
- Smith SW. Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents. Dr. Smithâ€™s ECG Blog, published 12 February 2012. [Free Full Text]
- Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats. Cleve Clin J Med. 2011; 78(6):404-14. [Free Full Text]